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What are the 7 important things to ask while taking a patient's history?

1. Duration—how long has the patient had the problem?
2. Reason—why are they there to see you and how did the problem happen if there was an event that caused it
3. Frequency
4. Location
5. Onset
6. Pain
7. Signs and symptoms

o Best seen after dilation of the pupil
o Look through direct ophthalmoscope held about 6 inches from patients eye or by using a slit lamp biomicroscope

how are cataracts txed?

o Early nuclear cataract: change glasses prescription
o Small central opacities: pupillary dilation may improve vision, but usually cannot be used as a long-term treatment option
o Cataract surgery: replacement of lens with implant

• Results from ischemia
• Angiogenic factors released cause neovascularization
• Can occur at the optic nerve (high risk condition) or at any location in the retina or at the iris causing neovascular glaucoma

what are the symptoms of Proliferative diabetic retinopathy?

• May be 20/20 – therefore, patient must be screened
• Vision decrease is slow or sudden
• Floaters - possible vitreous hemorrhage, described as “shower”
• Blind spots in the vision

• The diabetic control and complications trial has shown that tight glycemic control decreases the progression of diabetic retinopathy, nephropathy, and neuropathy
• The clinician’s (our) role is essential
• Prompt referral indicated
• Retinal Laser photocoagulation – localized destruction of the retina to prevent spread of pathology

what is Diabetic Macular Edema?

• Earliest detectable clinical change in vasculature is the formation of microaneurisms
• Fluid leaks into retinal tissue and may accumulate in foveal area which leads to decreased visual acuity

what are the sxs of diabetic macular edema?

• May have none, but still require laser treatment
• Possible decreased vision: may be unilateral or bilateral

-May involve central retinal artery (CRAO) or a branch of the central retinal artery (BRAO)
-Unilateral involvement may only be noticeable after the patient closes the uninvolved eye – they may not realize the deficit
-Cilioretinal arteries supply a portion of the macula in up to 20% of persons – may save central vision if a problem occurs
-Retinal whitening may fade with time
-CRAO may cause ischemia to the macula
-A soft glistening yellow embolus conforming to the blood vessel lumen or forming a Y-shaped obstruction at a branch point is usually a cholesterol embolus (Hollenhorst plaque) that arises from the carotid arteries
-A hard, whitish plaque may represent a calcific embolus from an abnormal heart valve

what are the sxs of retinal artery occlusion?

-A sudden, painless unilateral loss in vision and -A sudden, painless visual field loss corresponds to a horizontal hemifield in cases of BRAO, ex. A superior BRAO causes an inferior field defect
-Amaurosis fugax (transient loss of vision) – implies an impending CRAO or BRAO with a classic description of a curtain descending over vision that clears over several minutes

what are the sns of retinal artery occlusion?

-A relative afferent pupillary defect is present (also know the term consensual response)
-If seen within first few hours of onset may not yet see retinal edema
-Embolus may be seen at level of optic nerve in CRAO
-Embolus may be seen at a branch point of an arteriole in BRAO
-Cherry red spot – a classic sign
-Arcuate retinal whitening corresponds to retinal distribution of occluded vessel
-Segmentation or boxcarring of retinal vessels
-Cilioretinal sparing may be present, if fortunate

-Evaluate- age of patient, any known systemic conditions
-Auscultate carotid arteries and heart listening for bruits or murmurs
-If patient is over 55, inquire about giant cell arteritis symptoms
-Neurologic history and exam
-Carotid ultrasound or angiography
-Cardiac echography
-Lab eval. Modified for each patient

-Relative afferent pupillary defect most commonly in cases of ischemic CRVO
-Blood and thunder fundus (compare to RAO, where there is whitening seen instead)
-Dilated and tortuous veins
-Flame-shaped hemorrhage
-Vitreous hemorrhage may occur
-Cotton wool spots
-Macular edema
-Exudates common
-Neovascularization of retina and iris

what is the workup for retinal vein occlusion?

-Evaluate for systemic hypertension
-Lab evaluation
-Test for thyroid eye disease and tumors- can cause compression of central retinal vein as it exits the eye

what is the tx for retinal vein occlusion?

-Mandatory ophthalmic exam within 48-72 hours of diagnosis
-BRVO with macular edema may result in decreased vision-laser photocoagulation
-Follow up- CRVO assessed every month for 6 months by the eye doc

what is Age Related Macular Degeneration (ARMD)?

-The most common cause of legal blindness in the western world
-Commonly affects individuals over age 65
-Cause is unknown
-Risk factors include older age, female gender, lighter pigmentation, and smoking
-May have a genetic component
-Degeneration of supporting structures of outer retina and photoreceptors responsible for deterioration of vision

what are the sns/sxs of ARMD?

-THE MOST COMMON abnormality seen is DRUSEN
-Drusen-yellowish deposits deep to the retina, may be small yellowish crystals or larger soft-yellow deposits
-Drusen may be localized to fovea or peripheral along arcades
-Deposits usually multicentric, giving the appearance of a bumpy fundus
-Drusen limit the nutritional and metabolic support to outer retina

what are the two types of ARMD?

-atrophic
-exudative

what is atrophic ARMD?

•AKA “dry” form
•more common
•Pallor (whitening) of macular area is seen

what is exudative ARMD?

•AKA “wet” form
•occurs as neovascularization which originates from choroidal vasculature, leaking fluid and lipid, which may bleed
•End-stage: large subretinal scar (disciform scar)

-Vitreous is only attached to the retina in two places – these can break with age
-Occurs in most individuals with time – fifth to seventh decade of life
-Occurs more often in highly myopic individuals – earlier age
-Retinal tears or breaks may occur

what is the sx of posterior vitreous detachment?

-Flashing lights and/or floaters

what is the tx for posterior vitreous detachment?

-Indirect ophthalmoscopy must be performed within 24 hours
-No treatment indicated
-Laser or cryotherapy if any new retinal tears or breaks

what is retinal detachment?

-Occurs when fluid separates the retina from the underlying pigment epithelium
-Several types (not discussed in this lecture)

what are the sxs of retinal detachment?

-Flashes and floaters
-Visual field loss described as a curtain, shadow or bubble of fluid
-Metamorphopsia
-Decreased vision

what are the sns of retinal detachment?

-Relative afferent pupillary defect
-Visual field loss unilateral, unless traumatic
-May be sectoral, quadrantic, hemifield, or total
-Retinal hydration lines, or rugae, have an appearance like ripples on a pond

what is the workup for retinal detachment?

-Difficult to diagnose with direct ophthalmoscopy
-Simple technique with a direct opththalmoscope to compare the reflexes of the two eyes
-An eye with a retinal detachment may have a lighter colored reflex (yellow or orange)

what is the tx for retinal detachment?

-Refer for immediate evaluation
-Surgical intervention necessary – retinal detachment may lead to blindness if not treated

•Flows past the lens, around the iris, into Schlemm’s canal via the trabecular meshwork, and then into aqueous and episcleral veins

what is glaucoma?

-Damage from glaucoma is manifested by optic nerve cupping which results in characteristic patterns of visual field loss
-Classically respects the horizontal meridian
-Visual acuity and central field remain normal until late in the disease process – may take some time before patient realizes this loss

-Frequency of disorder increases with each decade
-Rare younger than 50, occasional from 50-59, more often over 60
-Pale optic disc swelling or only minimal disc changes out of proportion to vision loss
-Temporal arteries often firm, tender or pulseless
-Sed rate is usually greater than 50, but can be normal
-Mild anemia is common
-Third, fourth or sixth cranial nerve palsy may occur
-Vision loss from central retinal artery occlusion can occur
-Relative afferent pupillary defect in unilateral cases
-Vision loss is caused by vasculitic occlusion of arteries to the optic disc

-Immediate corticosteroid; IV methylprednisolone 250 mg every 6 hours for 3 days with acute vision loss followed by oral, daily doses
-or-
-Prednisone 80-100 mg orally if GCA suspected but no vision loss has occurred
-Follow-up with a second biopsy of contralateral temporal artery if first biopsy negative but strong clinical suspicion
-Long term corticosteroids with slow taper requires careful monitoring for side effects

what are the sxs of optic neuritis?

-a unilateral vision loss over several days
-Pain with movement of eyes
-Transient neurologic disturbances
-Spontaneous recovery over weeks

what are the sns of optic neuritis?

-2/3 of patients have initially normal appearing discs, 1/3 have disc edema
-Central field loss common
-Relative afferent pupillary defect but may be absent
-Spontaneous near complete recovery within months

-Ophthalmic evaluation
-MRI of brain and orbits with contrast
-CBC, electrolytes and chest x-ray if corticosteroids

what is the tx for optic neuritis?

-White matter plaques found on MRI= IV methylprednisilone (250mg) every 6 hours for 3 days (optional 10 day oral taper)
-Without white matter changes, IV steroids have no proven long-term advantage but often used in ONE EYED patients or those with severe vision loss

Inspect the skin around the eye, lids, lid margins, conjunctiva, presence or absence of d/c, preauricular adenopathy, lice on the eye lids.
-prognosis is better for patients who can detect SOME light through an injured eye than no light at all

magnification of structures anterior to the iris, including the anterior chamber, cornea, and conjunctiva, foreign bodies in the cornea or conjunctiva. Better assessment of corneal defects/infiltrates than the ophthalmoscope.

why is lid eversion useful?

identifies foreign bodies under the upper lid. Single and double lid inversion. Need special retractor

what is the tool used for measurement of IOP?

Tonometry

what is a NL IOP?

12-21 mmHg

what are other ways to measure IOP?

-Goldmann-type application tonometer- gold standard requires significant training and skill / eye specialist.
-Tonopen: Commonly used by GPs, EPs, FDs as screening tool.
-Shiotz tonometer: Metal tonometer / mechanically indents the cornea. With this instrument, the lower the measurement, the higher the pressure. It is cumbersome to use. Patient must be supine. This method is rarely used
-Eye ballottement: gentle palpation of both eyes in the setting of acute angle-closure glaucoma /one eye is harder than the unaffected eye.

what is seen in a direct funduscopy exam?

uses ophthalmoscope. Can see only central area of retina, disc, macula. Cannot see periphery.

what is seen in an indirect funduscopy exam?

done by eye specialist. Allows visualization of retina periphery. Able to pick up early retinal detachments as most start at the periphery and are not visible with the ophthalmoscope.

what is conjunctivitis?

Injected conjunctiva - red eye & purulent D/C usually starts in one eye, but spreads to the other in 48 hrs.

Edge of the eyelid turns inward so eyelashes rub on the cornea.
-due to age, also scarring of conjunctiva from chronic infection - Trachoma
-Painful and can cause scarring of cornea & blindness.

what is the tx for entropion?

surgery

what is Ectropion?

Lower eyelid sags away from eyeball, like a bloodhound..
-Causes, old age, paralysis of facial muscles like Bell’s Palsy.
-Exposed conjunctiva can become inflamed.

what is the tx for ectropion?

surgery

what is acute vision loss?

-Divide pts by age and type of vision loss. Partial loss or complaints of flashing lights or floaters suggests retinal detachment.
-Nontraumatic vision loss under age 50 is almost always due to optic neuritis (symptom of MS). Over age 60, vascular causes predominate with temporal arteritis rarely occurring before age 65

what is Acute Vision Loss Under Age 50: Optic Neuritis (ON)?

-occurs between age 15 -45. Rapid over hours, maximal at 2 weeks
-Vision loss w/ alteration in color vision.
-Classically it is said w/ ON: the patient doesn’t see anything and the doctor doesn’t see anything.
-DX: decreased vision and afferent pupillary defect.
-association of ON w/ Multiple Sclerosis

-causes vision loss, mostly central and critical detailed vision. Disease of the elderly, slow and progressive over many years
-scattered pale dots, spots, or modeling on the macular (called drusen)
-2 types, wet and dry
-Wet = leakage of fluid or blood around the central fovea, can be treated with laser

what is Amblyopia?

Subnormal visual acuity in one or both eyes despite appropriate correction of any significant refractive error

-Functional: No pathologic alteration of the retina or visual pathways. Vision impairment is due to deprivation of sensory stimulation (disuse) or to inhibition (misuse). Most common cause is strabismus, in which the amblyopia results from the lack of use or active suppression of macular vision in the deviating eye.

what is Strabismus?

(imbalance of extraocular muscles)
-common in infants and young children
-may be a sign of serious eye disease
-may cause amblyopia

what is papilledema?

(edema and inflammation of the optic nerve at its point of entrance into the eyeball)
-etiology increased intracranial pressure often cause by tumor of the brain, infections such as meningitis or encephalitis pressing on the optic nerve
-blindness may result very rapidly unless relieved

what is retinal detachment? TX?

-sudden flashes of light or shower of floaters in infected eye
-risks are high myopia, previous detachment in either eye, trauma, cataract operation without lens implant
-often begin at the periphery but if they involve the macula can lead to loss of vision. TX: laser

-Do not repair.
-Refer to ophthalmologist.
-Require 3 stitch closure under magnification to prevent a lid notch.
-Medial lid lac: Must r/o nasolacrimal system injury. (fluorescene stained saline injected via punctum and look for appearance in the wound.
- Upper lid lacerations can damage the levator muscle /aponeurosis. If so, it should be repaired in OR to prevent ptosis.

what are Corneal/sclera lacerations?

-Assess by “painting” the laceration w/ fluorescence and look for streaming of fluorescence from the wound.
-Avoid unnecessary pressure on the globe. Refer to ophthalmologist.

what are Severed extraocular muscles?

-rare but difficult problem
-Can lead to permanent strabismus.

what is a Retained intraocular foreign body?

-FB can enter the globe leaving little evidence of penetration.
-Suspect with history of metal on metal, grinding
-Ways to identify/localize FB: Direct visualization( Slit lamp, ophthalmoscopy), orbital x-rays, CT scan, Ultrasound, MRI( but avoid if metal is suspected).
-The presence of more than 1 FB must be considered.
-Refer to ophthalmologist for removal.